International Team Led By IGeneX Laboratories And Union Square Medical Associates Supports Link Between Borrelia Spirochetes And Mysterious Skin Disease

Morgellons Lesions on Patient’s Legs

We hope that new tests for Borrelia will lead to better treatment for Morgellons patients

PALO ALTO, Calif. (PRWEB) November 13, 2018

Morgellons disease is frequently associated with Borrelia burgdorferi (Bb), the agent of Lyme disease, as well as tickborne relapsing fever Borrelia (RFB) according to a study published in the prestigious journal Clinical Cosmetic and Investigational Dermatology (https://bit.ly/2SVRT8h). The report entitled “Detection of Tickborne Infection in Morgellons Disease Patients by Serological and Molecular Techniques” was written by microbiologist Marianne Middelveen from Atkins Veterinary Services in Calgary, Canada, together with laboratory director Jyotsna Shah and technologist Iris Du Cruz of IGeneX Laboratories in Palo Alto, CA, and nurse practitioner Melissa Fesler and internist Raphael Stricker from Union Square Medical Associates in San Francisco, CA.

Morgellons disease is a bizarre skin condition previously linked to tickborne disease. It features lesions containing black, white or multicolored filaments. Many physicians mistakenly believe the filaments are implanted textile fibers and that the condition is a form of delusional mental illness.

Morgellons Lesions on Patient’s Back

“Erroneous beliefs of medical professionals have impeded diagnosis and treatment in this group of patients”, explains Middelveen.

Borrelia organisms including Bb and RFB comprise a family of corkscrew-shaped bacteria called spirochetes. In this corroborative study, 90% of the Morgellons patients tested positive for Borrelia spirochetes.Among these patients with skin disease, 23% were positive for Bb alone, 50% for RFB alone, and 17% for both.

“This is a huge percentage compared to the general population”, says Fesler.

In addition, infection with another tickborne pathogen, Bartonella henselae, was detected in 20% of the Morgellons study subjects and strengthens the evidence linking the skin condition to tickborne illness.

“This study is another nail in the coffin for the delusionists”, adds Stricker.

Many clinicians are unaware of the full spectrum of Borrelia spirochetes that are associated with Morgellons disease.

“Testing for a diverse group of organisms is an ongoing challenge”, says Du Cruz.

To further complicate diagnostic hurdles, Lyme disease testing as recommended by the Centers for Disease Control and Prevention (CDC) lacks sensitivity and there are currently no tests for RFB that are approved by the Food and Drug Administration (FDA) in the United States.

“The genetic complexity of Borrelia infection highlights the need for better testing”, says Shah. “We hope that new tests for Borrelia will lead to better treatment for Morgellons patients.”

Abstract
There is insufficient evidence to support screening of various tick-borne diseases (TBD) related microbes alongside Borrelia in patients suffering from TBD. To evaluate the involvement of multiple microbial immune responses in patients experiencing TBD we utilized enzyme-linked immunosorbent assay. Four hundred and thirty-two human serum samples organized into seven categories followed Centers for Disease Control and Prevention two-tier Lyme disease (LD) diagnosis guidelines and Infectious Disease Society of America guidelines for post-treatment Lyme disease syndrome. All patient categories were tested for their immunoglobulin M (IgM) and G (IgG) responses against 20 microbes associated with TBD.Our findings recognize that microbial infections in patients suffering from TBDs do not follow the one microbe, one disease Germ Theory as 65% of the TBD patients produce immune responses to various microbes. We have established a causal association between TBD patients and TBD associated co-infections and essential opportunistic microbes following Bradford Hill’s criteria. This study indicated an 85% probability that a randomly selected TBD patient will respond to Borrelia and other related TBD microbes rather than to Borrelia alone.

A paradigm shift is required in current healthcare policies to diagnose TBD so that patients can get tested and treated even for opportunistic infections.

Please see link for full article. Snippets below:

Introduction
Tick-borne diseases (TBDs) have become a global public health challenge and will affect over 35% of the global population by 20501. The most common tick-borne bacteria are from the Borrelia burgdorferi sensu lato (s.l.) group. However, ticks can also transmit co-infections like Babesia spp.2, Bartonella spp.3, Brucella spp.4,5,6,7,8, Ehrlichia spp.9, Rickettsia spp.10,11, and tick-borne encephalitis virus12,13,14. In Europe and North America, 4–60% of patients with Lyme disease (LD) were co-infected with Babesia, Anaplasma, or Rickettsia11,15,16. Evidence from mouse and human studies indicate that pathogenesis by various tick-borne associated microbes15,16,17 may cause immune dysfunction and alter, enhance the severity, or suppress the course of infection due to the increased microbial burden18,19,20,21,22. As a consequence of extensive exposure to tick-borne infections15,16,17, patients may develop a weakened immune system22,23, and present evidence of opportunistic infections such as Chlamydia spp.24,25,26,27, Coxsackievirus28, Cytomegalovirus29, Epstein-Barr virus27,29, Human parvovirus B1924, and Mycoplasma spp.30,31. In addition to tick-borne co-infections and non-tick-borne opportunistic infections, pleomorphic Borrelia persistent forms may induce distinct immune responses in patients by having different antigenic properties compared to typical spirochetes32,33,34,35. Nonetheless, current LD diagnostic tools do not include Borrelia persistent forms, tick-borne co-infections, and non-tick-borne opportunistic infections.

The two-tier guidelines36,37,38 for diagnosing LD by the Centers for Disease Control and Prevention (CDC) have been challenged due to the omission of co-infections and non-tick-borne opportunistic infections crucial for comprehensive diagnosis and treatment39,40. Emerging diagnostic solutions have demonstrated the usefulness of multiplex assays to test for LD and tick-borne co-infections41,42. However, these new technologies do not address seroprevalence of non-tick-borne opportunistic infections in patients suffering from TBD and they are limited to certain co-infections41,42. Non-tick-borne opportunistic microbes can manifest an array of symptoms24,29 concerning the heart, kidney, musculoskeletal, and the central nervous system as seen in patients with Lyme related carditis43, nephritis44, arthritis45, and neuropathy46, respectively. Therefore, Chlamydia spp., Coxsackievirus, Cytomegalovirus, Epstein-Barr virus, Human parvovirus B19, Mycoplasma spp., and other non-tick-borne opportunistic microbes play an important role in the differential diagnosis of LD24,29. As the current knowledge regarding non-tick-borne opportunistic microbes is limited to their use in differential diagnosis of LD, it is unclear if LD patients can present both tick-borne co-infections and non-tick-borne opportunistic infections simultaneously.

For the first time, we evaluate the involvement of Borrelia spirochetes, Borrelia persistent forms, tick-borne co-infections, and non-tick-borne opportunistic microbes together in patients suffering from different stages of TBD. To highlight the need for multiplex TBD assays in clinical laboratories, we utilized the Bradford Hill’s causal inference criteria47 to elucidate the likelihood and plausibility of TBD patients responding to multiple microbes rather than one microbe. The goal of this study is to advocate screening for various TBD microbes including non-tick-borne opportunistic microbes to decrease the rate of misdiagnosed or undiagnosed48 cases thereby increasing the health-related quality of life for the patients39, and ultimately influencing new treatment protocol for TBDs.

In Fig. 2A, 51% and 65% of patients had IgM and IgG responses to more than one microbe, whereas 9% and 16% of patients had IgM and IgG responses to only one microbe, respectively. Immune responses to Borrelia persistent forms (all three species) for IgM and IgG were 5–10% higher compared to Borrelia spirochetes in all three species (Fig. 2B). Interestingly, the probability that a randomly selected patient will respond to Borrelia persistent forms rather than the Borrelia spirochetes (Fig. S2) is 80% (d = 1.2) for IgM and 68% for IgG (d = 0.7). Figure 2A and B indicated that IgM and IgG responses by patients from different stages of TBDs are not limited to only Borrelia spirochetes.

In Fig. 3 sub-inlets, more than 50% of the patients reacted to only the individual Borrelia strains suggesting that Borrelia antigens are not cross-reactive. If patients were cross-reacting among antigens, a larger percentage of the patients would be seen with the combination of all three species (Fig. S2). These results provide evidence to suggest that the inclusion of different Borrelia species and their morphologies in current LD diagnostic tools will improve its efficiency.

Discussions
The study outcome indicated that polymicrobial infections existed at all stages of TBD with IgM and IgG responses to several microbes (Fig. 2). Results presented in this study propose that infections in patients suffering from TBDs do not obey the one microbe one disease Germ Theory. Based on these results and substantial literature11,15,16,17,27,49,50,51 on polymicrobial infections in TBD patients, we examined the probability of a causal relationship between TBD patients and polymicrobial infections following Hill’s nine criteria47.

An average effect size of d = 1.5 for IgM and IgG (Fig. 4A) responses is considered very large52. According to common language effect size statistics53, d = 1.5 indicates 85% probability that a randomly selected patient will respond to Borrelia and other TBD microbes rather than to only Borrelia. Reports from countries such as Australia27, Germany49, Netherlands11, Sweden50, the United Kingdom51, the USA15,16, and others indicate that 4% to 60% of patients suffer from LD and other microbes such as Babesia microti and human granulocytic anaplasmosis (HGA). However, previous findings11,15,16,27,49,50,51 are limited to co-infections (i.e., Babesia, Bartonella, Ehrlichia, or Rickettsia species) in patients experiencing a particular stage of LD (such as Erythema migrans). In contrast, a broader spectrum of persistent, co-infections, and opportunistic infections associated with diverse stages of TBD patients have been demonstrated in this study (Fig. 2). From a clinical standpoint, the likelihood for IgM and IgG immune responses by TBD patients to the Borrelia spirochetes versus the Borrelia persistent forms, and responses to just Borrelia versus Borrelia with many other TBD microbes has been quantified for the first time (Fig. S2).

Borrelia pathogenesis could predispose individuals to polymicrobial infections because it can suppress, subvert, or modulate the host’s immune system18,19,20,21,22 to create a niche for colonization by other microbes54. Evidence in animals55 and humans11,15,16,27,49,50,51 frequently indicate co-existence of Borrelia with other TBD associated infections. Interestingly, IgM and IgG immune levels by patients to multiple forms of Borrelia resulted in immune responses to 14 other TBD microbes (Fig. 4B). In contrast, patient responses to either form of Borrelia (spirochetes or persistent forms) resulted in reactions to an average of 8 other TBD microbes (Fig. 4B). Reaction to two forms of Borrelia reflected an increase in disease severity indicating biological gradient for causation as required by Hill’s criteria47.

Multiple microbial infections in TBD patients seem plausible because ticks can carry more than eight different microbes depending on tick species and geography56,57. Moreover, Qiu and colleagues reported the presence of at least 18 bacterial genera shared among three different tick species and up to 127 bacterial genera in Ixodes persulcatus58. Interestingly, research indicates Chlamydia-like organism in Ixodes ricinus ticks and human skin59 that may explain immune responses to Chlamydia spp., seen in this study (Fig. 2). Additionally, prevalence of TBD associated co-infections such as B. abortus, E. chaffeensis, and opportunistic microbes such as C. pneumoniae, C. trachomatis, Cytomegalovirus, Epstein-Barr virus, and M. pneumoniae have been recorded in the general population of Europe and the USA (Table S2). However, true incidence of these microbes is likely to be higher considering underreporting due to asymptomatic infections and differences in diagnostic practices and surveillance systems across Europe and in the USA. More importantly, clinical evidence for multiple microbes has been reported in humans11,15,16,27,49,50,51, and livestock55 to mention the least. Our findings regarding the presence of polymicrobial infections at all stages of TBD further supports the causal relationship between TBD patients and polymicrobial infections (Fig. 2). Various microbial infections in TBD patients have been linked to the reduced health-related quality of life (HRQoL) and increased disease severity39.

An association between multiple infections and TBD patients relates well to other diseases such as periodontal, and respiratory tract diseases. Oral cavities may contain viruses and 500 different bacterial species60. Our findings demonstrate that TBD patients may suffer from multiple bacterial and viral infections (Fig. 4). In respiratory tract diseases, influenza virus can stimulate immunosuppression and predispose patients to bacterial infections causing an increase in disease severity61. Likewise, Borrelia can induce immunosuppression that may predispose patients to other microbial infections causing an increase in disease severity.

Traditionally, positive IgM immune reaction implies an acute infection, and IgG response portrays a dissemination, persistent or memory immunity due to past infections. Depending on when TBD patients seek medical advice, the level of anti-Borrelia antibodies can greatly vary as an Erythema migrans (EM) develops and may present with IgM, IgG, collective IgM/IgG, or IgA62. This study recommends both IgM and IgG in diagnosing TBD (Figs 5 and S4–S6) as unconventional antibody profiles have been portrayed in TBD patients. Presence of long-term IgM and IgG antibodies have been reported in LD patients that were tested by the CDC two-tier system. In 2001, Kalish and colleagues reported anti-Borrelia IgM or IgG persistence in patients that suffered from LD 10–20 years ago63. Similarly, Hilton and co-workers recorded persistent anti-Borrelia IgM response in 97% of late LD patients that were considered cured following an antibiotic treatment64.

Similar events of persistent IgM and IgG antibody reactions were demonstrated in patients treated for Borrelia arthritis and acrodermatitis chronica atrophicans65, chronic cutaneous borreliosis66, and Lyme neuroborreliosis67. A clear phenomenon of immune dysfunction is occurring, which might account for the disparities in LD patient’s antibody profiles and persistence. Borrelia suppresses the immune system by inhibition of antigen-induced lymphocyte proliferation18, reducing Langerhans cells by downregulation of major histocompatibility complex class II molecules on these cells19, stimulating the production of interleukin-10 and anti-inflammatory immunosuppressive cytokine20, and causing disparity in regulation and secretion of cytokines21. Other studies have demonstrated low production or subversion of specific anti-Borrelia antibodies in patients with immune deficiency status22.

In the USA alone, the economic healthcare burden for patients suffering from LD and ongoing symptoms is estimated to be $1.3 billion per year69. Additionally, 83% of all TBD diagnostic tests performed by the commercial laboratories in the USA accounted for only LD70. Globally, the commercial laboratories’ ability to diagnose LD has increased by merely 4% (weighted mean for ELISA sensitivity 62.3%) in the last 20 years71. This study provides evidence regarding polymicrobial infections in patients suffering from different stages of TBDs. Literature analyses and results from this study followed Hill’s criteria indicating a causal association between TBD patients and polymicrobial infections. Also, the study outcomes indicate that patients may not adhere to traditional IgM and IgG responses.

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**Comment**

For the first time, Garg et al. show a 85% probability for multiple infections including not only tick-borne pathogens but also opportunistic microbes such as EBV and other viruses.

I’m thankful they included Bartonella as that one is often omitted but definitely a player. I’m also thankful for the mention of viruses as they too are in the mix. The mention of the persister form must be recognized as well as many out there deny its existence.

Key Quote: “Our findings recognize that microbial infections in patients suffering from TBDs do not follow the one microbe, one disease Germ Theory as 65% of the TBD patients produce immune responses to various microbes.”

August, 2018: Nymphal deer ticks are less abundant but still active in Wisconsin right now. About 20-25% of nymphs are infected with the Lyme spirochete. Overall, 2018 has been normal in terms of tick numbers.

NEW for 2018: We are starting a tick identification service. Identifying the stage and species of a tick are crucial to deciding whether to seek medical attention or not. Tick-borne diseases are only carried by certain ticks in specific regions. We can help you identify the tick you’ve found based on your images and geographical location. Use the following link to submit your photos and information:

There is also a tab titled “Tick-Borne Diseases.” Go to link to read about them. They give WI stats as well. Please remember ALL the numbers are low as many go unreported:

Lyme (Bb or Bm)

Borrelia miyamotoi (relapsing fever)

Anasplasmosis

Ehrlichia muris eauclairensis (EML)

Babesiosis

Powassan virus/deertick virus

Ehrlichia chaffeensis

Rocky Mountain Spotted Fever

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A few points stick out to me:

Please take pictures of these ticks & send them in so we finally have an accurate record. They are asking us for help so let’s give it. It will only help us in the end. Flood them with ticks!

Baronella didn’t make the list, yet nearly everyone I work with has it. WHY? Because while Bart has been found in ticks, it hasn’t been proven conclusively they transmit. Bart is a nasty, nasty bug and alone can kill you. Coupled with Lyme it can make you want to die.

The lack of data is glaring. Seriously. Glaring. Zika makes front page news here and our mosquitoes can’t even carry it. https://madisonarealymesupportgroup.com/2018/03/13/wed-nite-the-lab-talk-on-mosquitoes-ticks-disease/ There were only 46 cases of Zika in the U.S. in 2018 – ALL due to travelers returning from affected areas.The CDC “estimates” that there are 300,000 NEW Lyme Disease cases annually in the U.S. Anyone see a disparity here between Zika and Lyme? (Other tick-borne diseases aren’t even on the radar yet)

Abstract

Borrelia are tick-borne bacteria that in humans are the aetiological agents of Lyme disease and relapsing fever. Here we present the first genomes of B. turcica and B. tachyglossi, members of a recently described and rapidly expanding Borrelia clade associated with reptile (B. turcica) or echidna (B. tachyglossi) hosts, transmitted by hard ticks, and of unknown pathogenicity.Borrelia tachyglossi and B. turcica genomes are similar to those of relapsing fever Borrelia species, containing a linear ~ 900 kb chromosome, a single long (> 70 kb) linear plasmid, and numerous short (< 40 kb) linear and circular plasmids, as well as a suite of housekeeping and macronutrient biosynthesis genes which are not found in Lyme disease Borrelia. Additionally, both B. tachyglossi and B. turcica contain paralogous vsp and vlp proteins homologous to those used in the multiphasic antigen-switching system used by relapsing fever Borrelia to evade vertebrate immune responses, although their number was greatly reduced compared to human-infectious species. However, B. tachyglossi and B. turcica chromosomes also contain numerous genes orthologous to Lyme disease Borrelia-specific genes, demonstrating a unique evolutionary, and potentially phenotypic link between these groups.Borrelia tachyglossi and B. turcica genomes also have unique genetic features, including degraded and deleted tRNA modification genes, and an expanded range of macronutrient salvage and biosynthesis genes compared to relapsing fever and Lyme disease Borrelia. These genomes and genomic comparisons provide an insight into the biology and evolutionary origin of these Borrelia, and provide a valuable resource for future work.

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**Comment**

We don’t hear much about the importance of reptiles but we should. According to independent Canadian tick researcher, too much emphasis has been placed on the white footed mouse and not enough on reptiles,particularly in the West & South. https://madisonarealymesupportgroup.com/2018/08/13/study-shows-lyme-not-propelled-by-climate-change/Scott has shown that there are established populations of deer ticks in Manitoba as well as in insular, hyper-endemic Corkscrew Island, yet both are devoid of white-footed mice. He points out that there are numerous reservoir hosts that must be considered including other mammals, birds, and reptiles.

This current abstract brings up Echidna – or spiny ant-eaters, yet another potential vector/reservoir which are egg-laying mammals.

Digging a bit further, I discovered that varieties of uniquely Australian borrelia have been identified and are in fact related to Relapsing fever and Reptilian fever groups found in the paralysis tick, a common tick that bites people. While the “powers that be” deny Lyme in Australia, this could be a way Australians are contracting a “Lyme-like” illness. http://karlmcmanus.org.au/borrelia-echidna-ticks/ (Abstract found in link)

The research possibilities are endless, but one things’s for certain, Australians are getting sick and there’s a reason why. To announce that Lyme doesn’t exist there is very short-sighted. Whether it’s Lyme caused by Bb or a “Lyme-like” illness caused by another organism, WE NEED TO KNOW, because in the sidelines are thousands of very sick people who deserve answers.

Abstract

In March 2017, a patient became febrile within 4 days after visiting a rustic conference center in Austin, Texas, USA, where Austin Public Health suspected an outbreak of tickborne relapsing fever a month earlier. Evaluation of a patient blood smear and molecular diagnostic assays identified Borrelia turicatae as the causative agent. We could not gain access to the property to collect ticks. Thus, we focused efforts at a nearby public park, <1 mile from the suspected exposure site. We trapped Ornithodoros turicata ticks from 2 locations in the park, and laboratory evaluation resulted in cultivation of 3 B. turicatae isolates. Multilocus sequencing of 3 chromosomal loci (flaB, rrs, and gyrB) indicated that the isolates were identical to those of B. turicatae 91E135 (a tick isolate) and BTE5EL (a human isolate). We identified the endemicity of O. turicata ticks and likely emergence of B. turicatae in this city.

Thankfully more and more is coming out revealing that in fact these poor patients and the doctors who dare to treat them are not delusional but are in fact dealing with tick borne illness. The Lyme-like illness that for all intents and purposes looks, smells, and acts just like Lyme, is caused by something that needs to be identified. We need to quit focusing on the red herring of climate change and start identifying these bugs so people can get better.

https://madisonarealymesupportgroup.com/2016/01/03/bartonella-treatment/ Various strains have been found in eye fluid, the heart (myocarditis and endocarditis), and cysts, and can infect by nearly anything puncturing the skin and exchanging bodily fluids – including needles. Evidence also suggests congenital transmission.…. Symptoms are largely associated with where the blood flow is compromised. The reason many have pain in the soles of their feet is due to inflammation caused by microvascular trauma. It has been known to cause cysts around dental roots leading to chronic and hard to diagnose head and face pain as well as root canals. This microvascular trauma is also to blame for brain issues causing psychological issues such as anxiety, anger, and suicidal thoughts, since the small vessel disease affects executive function. A cog is literally caught in the wheel. As neurotransmitters become depleted due to overstimulation, depression rears its ugly head. A vicious cycle ensues. Due to the cyclical nature of Bartonella and that it exists in very low amounts in human blood, blood tests are unreliable. It also has a long division time between 22-24 hours and requires a special growth environment. There is a Triple Draw through Galaxy which collects blood over 8 days to maximize the test, stating a 90% reduction in false negatives.